Non-steroid, anti-inflammatory drugs exert most of their anti inflammatory, analgesic and antipyretic activity and inhibit hormone-induced uterine concentrations and certain types of cancer growth through the inhibition of prostaglandin G/H synthase, also known as cyclooxygenase. Until recently, only one form of cyclooxygenease had been characterised, this corresponding to cyclooxygenase I or the constitutive enzyme, as originally identified in bovine seminal vesicles. Recently the gene for a second inducible form of cyclooxygenase (cyclooxygenase-2) has been cloned, sequenced and characterised from chicken, murine and human sources. This enzyme is distinct from the cyclooxygenease-1 which has now also been cloned, sequenced and characterised from sheep, murine and human sources. The second form of cyclooxygenase, cyclooxygenase-2 is rapidly and readily inducible by a number of agents including mitogens, endotoxins, hormones, cytokines and growth factors. As prostaglandines have both physiological and pathological roles, it was concluded that the constitutive enzyme, cyclooxygenase-1, is responsible, in large part, for endogenous basal release of prostaglandins and hence is important in their physiological functions such as the maintenance of gastrointestinal integrity and renal blood flow. In contrast it was also concluded that the inducible form of cyclooxygenase-2 is mainly responsible for the pathological affects of prostaglandins where rapid induction of the enzyme would occur in response to such agents as inflammatory agents, hormones, growth factors and cytokines. Thus, a selective inhibitor of cyclooxygenase-2 will have similar anti inflammatory, antipyretic and analgesic properties to a conventional non-steroidal anti inflammatory drug and in addition would inhibit hormone-induced uterine contractions and have potential anti cancer effects but will have a diminished ability to induce some of the mechanism based side effects. In particular such a compound should have a reduced potential for gasterointestinal toxicity, a reduced potential for renal side effects, a reduced effect on bleeding tomes and possibly a lessened ability to induce attacks of asthma in aspirin-sensitive asthmatic subjects.
4-(4-methyl thio phenyl)-3-phenyl-2(5H)-furanone of the formula II shown herein below:
is a key intermediate in the preparation of COX-II inhibitor, known in the art as Rofecoxib which has a structure X given below:

The process known in the art for preparing the intermediate compound of the formula II involve tedious multi-step synthesis, utilizing expensive reagents. Therefore, the known synthetic processes for the production of the compound of formula II is not economically viable and are not cost effective.
It has now been found that the novel compound of formula I can be used as a starting material for the production of the compound of formula II in an economically advantageous manner. Cost-effective preparation of this intermediate, no doubt helps in reducing the price line of COX II inhibitor.